Lysophosphatidylcholine acyltransferase 3 (LPCAT3) is known to play a pivotal role in lipid metabolism, but its role in the early brain injury (EBI) following subarachnoid hemorrhage (SAH) remains unclear. This study provides insights into LPCAT3 expression alterations and functional implications in EBI following SAH. SAH models of adult male Sprague-Dawley (SD) rats were established by intravascular perforation. Lentivirus vectors were administered by intracerebroventricular injection (i.c.v.) to either induce LPCAT3 overexpression or knockdown 14 days before SAH induction. Western blot, immunofluorescence, Nissl staining, MDA detection, ROS detection, iron content detection, and short-term and long-term neurobehavioral tests were performed to investigate the effects of regulated-LPCAT3 after SAH. LPCAT3 levels were found to be significantly elevated in SAH. Suppression of LPCAT3 expression via shRNA improved oxidative stress, reduced brain edema, alleviated behavioral and cognitive deficits following SAH and decreased neuronal death, while upregulating LPCAT3 expression showed opposing effects. LPCAT3 is involved in SAH-induced EBI and associated with ferroptosis. Our findings provide a referential basis for potential therapeutic interventions aimed at alleviating EBI following SAH.

中文翻译：

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LPCAT3 加剧大鼠蛛网膜下腔出血后早期脑损伤和铁死亡

已知溶血磷脂酰胆碱酰基转移酶 3 (LPCAT3) 在脂质代谢中发挥关键作用，但其在蛛网膜下腔出血 (SAH) 后早期脑损伤 (EBI) 中的作用仍不清楚。这项研究提供了对SAH后EBI中LPCAT3表达改变和功能影响的见解。采用血管内穿孔法建立成年雄性SD大鼠SAH模型。在 SAH 诱导前 14 天，通过脑室内注射 (icv) 施用慢病毒载体以诱导 LPCAT3 过表达或敲低。通过Western blot、免疫荧光、尼氏染色、MDA检测、ROS检测、铁含量检测以及短期和长期神经行为测试来研究调节性LPCAT3在SAH后的作用。发现 SAH 中 LPCAT3 水平显着升高。通过 shRNA 抑制 LPCAT3 表达可改善氧化应激，减少脑水肿，减轻 SAH 后的行为和认知缺陷，并减少神经元死亡，而上调 LPCAT3 表达则显示出相反的作用。 LPCAT3 参与 SAH 诱导的 EBI 并与铁死亡相关。我们的研究结果为旨在减轻 SAH 后 EBI 的潜在治疗干预措施提供了参考依据。